胃癌病人NK细胞活性变化机理的初步研究

应用~(51)Cr释放试验和效靶结合试验,同时测定了正常人和胃癌病人外周血NK细胞活性与靶结合细胞数(TBC),研究了正常人及病人血浆对NK细胞功能的影响。发现正常人NK细胞活性与靶结合细胞数之间的关系呈直线正相关,但在NK活性降低的病人中靶结合细胞数却无明显改变,二者无相关性,而病人的血浆对正常人外周血NK活性则有明显的抑制作用(P<0.05),且抑制率与胃癌人NK细胞活性存有着负相关的关系,提示胃癌病人血浆具有抑制NK细胞活性的物质。     

The estimation of the plasma free fraction of cyclosporine in rabbits and heart transplant patients: The application of a physiological model of renal clearance

We estimated the free fraction (f_u) of cyclosporine (CyA) in the plasma from concentrations of CyA in urine (C_u) and plasma (C_p), urine flow rate (UF), and glomerular filtration rate in rabbits and in heart transplant patients. Following intravenous administration of CyA (5–30 mg kg^?1) in ten NZW rabbits and oral administration of CyA (4.8–12.1 mg kg^?1) in nine heart transplant patients, CyA concentrations in urine and plasma were measured by HPLC. The ratios of C_u to C_p and UF data were fitted to a physiological model of renal clearance using NONMEM. The free fraction of cyclosporine in the rabbits and the heart transplant patients was 0.0122 and 0.14, respectively. Because of the relatively low permeability of CyA across the tubular epithelium, no apparent equilibrium between C_u and C_p at any urine flow rate was reached and, therefore, the C_u to C_p ratio will not be equal to f_u.     

浆细胞病患者IL-4产生细胞数减少的意义及机制探讨

本文运用APAAP法检测了16名浆细胞患者外周血细胞在PHA刺激下产生IL-4的能力。发现浆细胞病组阳性细胞比率明显低于正常对照组(P<0.001),且阳性细胞比率与患者血清中多克隆IgM、IgA水平呈正相关(r=0.806和r=0.703)。在正常人外周血中加入CRP50mg/L,经PHA刺激后IL-4产生细胞也明显减少。作者假设,由于IL-6增高引起CRP等急性期相蛋白大量分泌,使IL-4产生受到明显抑制,从而使B细胞激活发生障碍是浆细胞病中多克隆免疫球蛋白合成抑制的主要原因。     

利培酮对氯氮平血浓度影响的研究

目的　了解利培酮对氯氮平血浓度的影响及二药合用的疗效与不良反应。方法　对 5 0例原服用氯氮平治疗的难治性精神分裂症患者合并利培酮治疗 ,分别于合并治疗前及后 1月、2月、3月测定氯氮平血浓度 ,同时评定PANSS ,TESS量表。结果　合用利培酮后 ,氯氮平血浓度无明显升高 ,PANSS评分明显降低(P <0 .0 1) ,TESS评分有所增加。结论　利培酮对氯氮平血浓度无明显影响 ,二药合用能增加疗效 ,不良反应有所增加。     

Sex differences in plasma cocaine levels and subjective effects after acute cocaine administration in human volunteers

Gender differences after acute cocaine administration have received little attention in spite of the fact that males and females respond differently to many drugs. Seven male and seven female occasional cocaine users received both an intranasal dose of cocaine hydrochloride (0.9 mg/kg) and placebo powder in a randomized order and reported subjective effects via an instrumental joystick device and various questionnaires. Blood samples were withdrawn at 5-min intervals to assess pharmacokinetic differences. Male subjects achieved the highest peak plasma cocaine levels (144.4 ± 17.5 ng/ml), detected cocaine effects significantly faster than females and also experienced a greater number of episodes of intense good and bad effects. Women studied during the follicular phase of their menstrual cycle had peak plasma cocaine levels of 73.2 ± 9.9 ng/ml, which was significantly higher than when they were studied during their luteal phase (54.7 ± 8.7 ng/ml), but there were no differences in their subjective reports of cocaine effects. In spite of the different cocaine blood levels and subjective effects, peak heart rate increases did not differ between males and females suggesting that women may be more sensitive than males to the cardiovascular effects of cocaine. These data suggest that there are significant gender and menstrual cycle differences in the response to acute intranasal cocaine administration and these differences may have implications for the differential abuse of this drug.This paper is dedicated to Xavier Lamas, MD, PhD, who lost his life while ascending Mt. Everest, August 1995     

Guillain-barré syndrome: A series observed at riyadh armed forces hospital january 1984–January 1994

A consecutive series of 47 hospitalized cases of Guillain-Barré syndrome seen over a 10-year period was analysed with respect to: (1) age and sex; (2) antecedent events and seasonal distribution; (3) patterns of clinical presentation; (4) CSF and neurophysiological findings; (5) results of treatment with plasma exchange; and (6) outcome. Twenty-two were children, 20 middle-aged and 5 aged; 37 were male and 10 were female. The most frequent antecedent event was upper respiratory tract infections; a seasonal peak incidence was found in winter. Clinical, CSF and neurophysiological findings concurred with those in the Western literature; 79% of the cases were severe. Plasma exchange performed within the first 2 weeks of onset benefitted in the short-term outcome, i.e. improvement by 1 grade at 4 weeks, but the long-term benefit, i.e. the ability to regain independent locomotion, was questionable. Plasma exchange helped in curtailing the time to walking unaided but had no benefit on the duration of artificial ventilation. Factors associated with an adverse outcome were: age over 15 years, severity of motor electrodiagnostic findings (especially a decreased distal CMAP amplitude and EMG signs of acute denervation), requirement for ventilation and slow progression (>3 weeks) to maximum deficit. After a mean follow-up of 11 months, 55% of the patients regained independent locomotion, which is a comparatively low proportion.     

The mechanism of yohimbine-induced renin release in the conscious rat

Summary These studies were designed to determine the role of the central nervous system, the sympathetic nervous system, the adrenal glands and the renal sympathetic nerves in yohimbine-induced renin release in conscious rats. Yohimbine (0.3–10 mg/kg, s.c.) caused time- and dose-related increases in plasma renin activity (PRA) and concentration (PRC) which were accompanied by time- and dose-related elevations of plasma norepinephrine (NE) and epinephrine (Epi) concentrations. Significant positive correlations were found between the increases in PRA and the increases in plasma NE and Epi concentrations caused by yohimbine, and propranolol (1.5 mg/kg, s.c.) blocked 90% of yohimbine (3 mg/kg, s.c.)-induced renin release. Over the entire spectrum of doses of yohimbine, the increases in PRA and plasma NE and Epi concentrations were positively correlated with the decreases in mean arterial pressure (MAP), but the -intercept was positive in every case and the 1 mg/ kg dose of yohimbine consistently increased PRA independent of any change in MAP. Complete renal denervation, as evidenced by a greater than 90% reduction in renal NE content, did not alter the increase in PRA caused by yohimbine (3 mg/kg, s.c.). An increase in circulating plasma catecholamine concentrations appeared to mediate yohimbine-induced renin release since propranolol prevented the rise in PRA caused by yohimbine in renal denervated rats. Prior adrenalectomy (Adx) also failed to prevent the rise in PRA produced by yohimbine (3 mg/kg, s.c.), but a combination of Adx and renal denervation caused a significant impairment of yohimbine-induced renin release. However, neither Adx alone nor the combination of Adx and renal denervation affected the increase in plasma NE concentration caused by yohimbine. Complete transection of the spinal cord at C₈ caused a drastic reduction in plasma catecholamine concentrations but did not change basal PRC. Yohimbine (3 mg/kg, s.c.) did not increase PRC or plasma catecholamine concentrations after spinal transection. Based on these results, we conclude that 1) the stimulation of renin release by yohimbine is a secondary neurohormonal consequence of the generalized increase in sympathetic activity caused by yohimbine, 2) the sympathoadrenal activation produced by yohimbine results from an action in the brain which is amplified by the simultaneous blockade of prejunctional ₂-adrenoceptors and 3) vasodepressor effects of the larger doses yohimbine cause a baroreflexly-mediated increase in sympathetic activity which interacts in a positive fashion with the central and peripheral sympathoexcitatory effects of yohimbine. Send offprint requests to T. K. Keeton     

Individual Differences in Plasma Catecholamine and Corticosterone Stress Responses of Wild-Type Rats: Relationship With Aggression

Plasma noradrenaline (NA), adrenaline (A), and corticosterone (CS) responses to social and nonsocial stressors were studied in male members of a strain of wild-type rats, widely differing in their level of aggression. The aggressiveness was preliminarily established by measuring the latency time to attack (ALT) a male intruder in a standard resident-intruder test. Animals were then provided with a jugular vein cannula for blood sampling during stress exposure. Implanted rats were randomly assigned to 3 experimental treatments: social stress (defeat experience, SD), nonsocial stress (presentation of a shock-prod, SP) and control (animals undisturbed in their home cages, CTR). A significant correlation was found between ALT and the amount of time spent in burying the probe in SP rats: the more aggressive the animal, the higher the rate of burying behavior. SD induced a much stronger effect on plasma NA, A, and CS concentrations than SP. A significant negative correlation was found between ALT scores and values of the area under the response time curve for NA and A, in both SD and SP situations: the more aggressive the animal, the higher the catecholaminergic reactivity to the stressors. On the contrary, no evidence of a correlation between aggressiveness and plasma corticosterone responses was found, neither in SD nor in SP rats. These findings in an unselected strain of wild-type rats confirmed that an aggressive/active coping strategy is associated with a high sympathetic-adrenomedullary activation and support the concept of individual differentiation in coping styles as a coherent set of behavioral and neuroendocrine characteristics.     

Fast-induced changes in plasma glucose, insulin and free fatty acid concentration compared in rats during the night and day

Changes in PG, PI and PFFA were examined and compared in fed rats or after 0 to 12 hours of fasting, during the night or during the day. At night, a progressive decrease in PG and PI and an increase in PFFA were induced by 0 to 12 hours of food deprivation. During the light period a decrease in PG occurred only from the 6th hour of fasting. A slight, progressive increase in PFFA levels was induced from 0 to 12 hours of fasting, while no significant variation of PI levels was observed. The results are discussed in terms of relationships between blood glucose, PFFA levels, and food intake in control rats over the circadian cycle.